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CBL0137

CAS No. : 1197996-80-7

MCE 國(guó)際站：CBL0137

產(chǎn)品活性：CBL0137 是一種 curaxin 化合物，是一種組蛋白伴侶促進(jìn)染色質(zhì)轉(zhuǎn)錄 (FACT) 抑制劑。CBL0137 下調(diào) NF-?B 并激活 p53。CBL0137 可恢復(fù)組蛋白 H3 乙�；�和三甲基化。CBL0137 是一種抗癌劑。CBL0137 誘導(dǎo)癌細(xì)胞凋亡 (apoptosis)。

研究領(lǐng)域：Epigenetics  |  Apoptosis  |  NF-κB

作用靶點(diǎn)：Histone Acetyltransferase  |  MDM-2/p53  |  NF-κB

In Vitro: Treatment with CBL-0137 leads to complete absence of living cells at concentrations above 2.5 μM. CBL-0137 causes a greater reduction in the number of colonies formed of not only MiaPaCa-2 cells when combined with gemcitabine, but also gemcitabine-resistant PANC-1 cells. Treatment of human pancreatic cancer cells with CBL-0137 results in a dose dependent reduction of protein and mRNA levels of RRM1 and RRM2. CBL-0137 is able to prevent gemcitabine induced expression of RRM1 and RRM2 on mRNA and protein levels.

In Vivo: The CBL-0137 monotherapy group and the CBL-0137-gemcitabine combination group samples show large necrotic fields, numerous apoptotic bodies and loss of tumor cells. Sub-optimal doses of 50 to 60 mg/kg CBL-0137 causes similar enhancement of gemcitabine antitumor activity as that produced by the maximum tolerated dose (MTD) of 90 mg/kg as indicated by the lack of statistically significant differences among the combination groups. CBL0137 hydrochloride inhibits FACT function through depletion of the pool of active FACT involved in transcription elongation. CBL-0137, given by oral gavage at a nontoxic dose of 30 mg/kg per day on a 5 days on/2 days off schedule, suppresses tumor growth in xenografts of colon (DLD-1), renal cell carcinoma (Caki-1), and melanoma (Mel-7) tumor cell lines and transplanted surgical samples from patients with pancreatic ductal adenocarcinoma.

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